The primary goal of this study is to assess the role of the sympathetic nervous system in the control of large vessel distensibility and small vessel resistance in the pulmonary circulation of conscious dogs. Dogs will be instrumented with catheters for the measurement of pulmonary artery (PA), left atrial (LA) and systemic arterial (SA) pressures (P), an electromagnetic flowprobe will be placed around the pulmonary artery for the measurement of blood flow and ultrasonic piezoelectric transducers will be sutured to opposing surfaces of the main, or branches of the pulmonary artery to measure PA dimensions. When the animals have fully recovered from surgery and are healthy and free from infection, the carotid chemoreflex will be stimulated with an intra-carotid injection of icotine (0.2 Mu g/kg) during the recording of pressures, pulmonary blood flow and pulmonary arterial dimensions. Pulmonary artery cross-sectional area and pulmonary vascular resistance will be calculated and used as indices of large vessel and small vessel vasoconstriction, respectively. Experiments will be repeated with ventilation controlled, with heart rate held constant, before and after Beta-adrenergic (propranolol), muscarinic (atropine) and Alpha-adrenergic (prazosin) receptor blockade, or after nerve section. Blood samples will be drawn simultaneously from the PA and LA for catecholamine analysis. Other cardiovascular reflexes, i.e. the coronary hypertensive chemoreflex (serotonin), the carotid baroreflex (bilateral carotid occlusion), and the aortic chemoreflex (nicotine) will also be used to activate pulmonary sympathetic vasomotor fibers. Whereas the sympathetic nervous systems has recognized effects on pulmonary vessel stiffness, the effects of sympathetic stimulation on pulmonary vascular resistance is uncertain and is thought to be trivial. This conclusion has limited the consideration and investigation of the role of the sympathetic nervous system in idiopathic pulmonary hypertension, pulmonary embolism, pulmonary hypertension associated with cerebral hypoxia and other changes in pulmonary vascular resistance. The present work will establish whether this conclusion is correct and will provide the basis for future studies of neural control of the pulmonary circulation.